Although the particles clearly induce pathways relevant to endothelial dysfunction (ET-1), carcinogenicity (CYP1A1), and metal toxicity (metallothionein-II), the exposures did not measurably initiate inflammation (wildtype) or exacerbate existing inflammation (TNF) in the lungs as measured by lavage cytology and global pulmonary gene expression. This evidence concerns the gene CYP1A1 and endothelial dysfunction.